Post-resistance exercise hypotension, hemodynamics, and heart rate variability: influence of exercise intensity

The occurrence of post-exercise hypotension after resistance exercise is controversial, and its mechanisms are unknown. To evaluate the effect of different resistance exercise intensities on post-exercise blood pressure (BP), and hemodynamic and autonomic mechanisms, 17 normotensives underwent three experimental sessions: control (C—40 min of rest), low- (E40%—40% of 1 repetition maximum, RM), and high-intensity (E80%—80% of 1 RM) resistance exercises. Before and after interventions, BP, heart rate (HR), and cardiac output (CO) were measured. Autonomic regulation was evaluated by normalized low- (LF_R–Rnu) and high-frequency (HF_R–Rnu) components of the R–R variability. In comparison with pre-exercise, systolic BP decreased similarly in the E40% and E80% (−6 ± 1 and −8 ± 1 mmHg, P < 0.05). Diastolic BP decreased in the E40%, increased in the C, and did not change in the E80%. CO decreased similarly in all the sessions (−0.4 ± 0.2 l/min, P < 0.05), while systemic vascular resistance (SVR) increased in the C, did not change in the E40%, and increased in the E80%. Stroke volume decreased, while HR increased after both exercises, and these changes were greater in the E80% (−11 ± 2 vs. −17 ± 2 ml/beat, and +17 ± 2 vs. +21 ± 2 bpm, P < 0.05). LF_R–Rnu increased, while ln HF_R–Rnu decreased in both exercise sessions. In conclusion: Low- and high-intensity resistance exercises cause systolic post-exercise hypotension; however, only low-intensity exercise decreases diastolic BP. BP fall is due to CO decrease that is not compensated by SVR increase. BP fall is accompanied by HR increase due to an increase in sympathetic modulation to the heart.     

Is the magnitude of acute post-exercise hypotension mediated by exercise intensity or total work done?

The purpose of this study was to investigate the effects of exercise intensity on the magnitude of acute post-exercise hypotension while controlling for total work done over the exercise bout. Seven normotensive physically active males aged 28 ± 6 years (mean ± SD) completed four experimental trials, a no exercise control, 30 min of semi-recumbent cycling at 70% (INT), cycling for 30 min at 40% (SMOD) and cycling at 40% for a time which corresponded to the same total work done as in the intense trial (LMOD). Blood pressure (BP), heart rate, stroke volume, cardiac output, total peripheral resistance, core body temperature and forearm skin and limb blood flow were measured prior to and for 20 min following the exercise bout. Post-exercise summary statistics were compared between trials with a one-factor general linear model. The change in systolic BP, averaged over the 20-min post-exercise period was significantly lower only following the INT (−5 ± 3 mm Hg) and LMOD exercise (−1 ± 7 mm Hg) compared to values in control (P < 0.04). The changes in systolic BP and MAP following INT and LMOD were not significantly different from each other (P > 0.05). Similar results were obtained when the minimum values of these variables recorded during the post-exercise period were compared. Mean changes in cardiac output (1.9 ± 0.3 l min⁻¹) and total peripheral resistance (−3 ± 1 mm Hg l⁻¹ min⁻¹) after INT exercise were also different from those in CON (P < 0.0005). The acute post-exercise reduction in BP was clinically similar following high intensity short duration exercise and moderate intensity longer duration exercise that was matched for total work done.     

Comparison of muscle buffer capacity and repeated-sprint ability of untrained, endurance-trained and team-sport athletes

We measured the muscle buffer capacity (βm) and repeated-sprint ability (RSA) of young females, who were either team-sport athletes (n=7), endurance trained (n=6) or untrained but physically active (n=8). All subjects performed a graded exercise test to determine followed 2 days later by a cycle test of RSA (5×6 s, every 30 s). Resting muscle samples (Vastus lateralis) were taken to determine βm. The team-sport group had a significantly higher βm than either the endurance-trained or the untrained groups (181±27 vs. 148±11 vs. 122±32 μmol H⁺ g dm⁻¹ pH⁻¹ respectively; P<0.05). The team-sport group also completed significantly more relative total work (299±27 vs. 263±31 vs. 223±21 J kg⁻¹, respectively; P<0.05) and absolute total work (18.2±1.6 vs. 14.6±2.4 vs. 13.0±1.9 kJ, respectively; P<0.05) than the endurance-trained or untrained groups during the RSA test. The team-sport group also had a greater post-exercise blood lactate concentration, but not blood pH. There was a significant correlation between βm and RSA (r = 0.67; P<0.05). Our findings show that young females competing in team sports have a larger βm than either endurance-trained or untrained females. This may be the result of the intermittent, high-intensity activity during training and the match play of team-sport athletes. The team-sport athletes also had a greater RSA than either the endurance-trained or untrained subjects. The greater total work by team-sport athletes was predominantly due to a better performance during the early sprints of the repeated-sprint bout.     

Post-concurrent exercise hemodynamics and cardiac autonomic modulation

Concurrent training is recommended for health improvement, but its acute effects on cardiovascular function are not well established. This study analyzed hemodynamics and autonomic modulation after a single session of aerobic (A), resistance (R), and concurrent (A + R) exercises. Twenty healthy subjects randomly underwent four sessions: control (C:30 min of rest), aerobic (A:30 min, cycle ergometer, 75% of VO₂ peak), resistance (R:6 exercises, 3 sets, 20 repetitions, 50% of 1 RM), and concurrent (AR: A + R). Before and after the interventions, blood pressure (BP), heart rate (HR), cardiac output (CO), and HR variability were measured. Systolic BP decreased after all the exercises, and the greatest decreases were observed after the A and AR sessions (−13 ± 1 and −11 ± 1 mmHg, respectively, P < 0.05). Diastolic BP decreased similarly after all the exercises, and this decrease lasted longer after the A session. CO also decreased similarly after the exercises, while systemic vascular resistance increased after the R and AR sessions in the recovery period (+4.0 ± 1.7 and +6.3 ± 1.9 U, respectively, P < 0.05). Stroke volume decreased, while HR increased after the exercises, and the greatest responses were observed after the AR session (SV, A = −14.6 ± 3.6, R = −22.4 ± 3.5 and AR = −23.4 ± 2.4 ml; HR, A =+13 ± 2, R =+15 ± 2 vs. AR =+20 ± 2 bpm, P < 0.05). Cardiac sympathovagal balance increased after the exercises, and the greatest increase was observed after the AR session (A = +0.7 ± 0.8, R = +1.0 ± 0.8 vs. AR = +1.2 ± 0.8, P < 0.05). In conclusion, the association of aerobic and resistance exercises in the same training session did not potentiate post-exercise hypotension, and increased cardiac sympathetic activation during the recovery period.     

Temporal association of elevations in serum cardiac troponin T and myocardial oxidative stress after prolonged exercise in rats

The objective of this study was to determine if prolonged exercise resulted in the appearance of cardiac troponin T (cTnT) in serum and whether this was associated with elevated levels of myocardial oxidative stress. Forty-five male Sprague–Dawley rats were randomized into four groups and killed before (PRE-EX), immediately (0HR), 2 (2HR) and 24 h (24HR) after a 3-h bout of swimming with 5% body weight attached to their tail. In all animals serum cTnT was assayed using 3rd generation electrochemiluminescence. In homogenized heart tissue myocardial malondialdehyde (MDA), a marker of lipid peroxidation, glutathione (GSH), and a non-enzymatic estimate of total antioxidant capacity (T-AOC) were assessed spectrophotometrically. At PRE-EX cTnT was undetectable in all animals. At 0HR (median, range: 0.055, 0.020–0.100) and 2HR post-exercise (0.036, 0.016–2.110) cTnT was detectable in all animals (P < 0.05). At 24HR post-exercise cTnT was undetectable in all animals. An elevation in MDA was observed 0HR (mean ± SD: 1.7 ± 0.2 nmol mgpro⁻¹) and 2HR (1.6 ± 0.3 nmol mgpro⁻¹) post-exercise compared with PRE-EX (1.3 ± 0.2 nmol mgpro⁻¹; P < 0.05). The antioxidant response to this challenge was a significant (P < 0.05) decrease in GSH 2HR and 24HR post-exercise. Despite this T-AOC did not alter across the trial (P > 0.05). The results indicated that prolonged and strenuous exercise in rats resulted in an elevation in cTnT, a biomarker of cardiomyocyte damage, in all animals 0HR and 2HR after exercise completion. The time course of cTnT elevation was temporally associated with evidence of increased lipid peroxidation in the rat heart.     

Oxidative stress, inflammation and recovery of muscle function after damaging exercise: effect of 6-week mixed antioxidant supplementation

There is no consensus regarding the effects of mixed antioxidant vitamin C and/or vitamin E supplementation on oxidative stress responses to exercise and restoration of muscle function. Thirty-eight men were randomly assigned to receive either placebo group (n = 18) or mixed antioxidant (primarily vitamin C & E) supplements (n = 20) in a double-blind manner. After 6 weeks, participants performed 90 min of intermittent shuttle-running. Peak isometric torque of the knee flexors/extensors and range of motion at this joint were determined before and after exercise, with recovery of these variables tracked for up to 168 h post-exercise. Antioxidant supplementation elevated pre-exercise plasma vitamin C (93 ± 8 μmol l⁻¹) and vitamin E (11 ± 3 μmol l⁻¹) concentrations relative to baseline (P < 0.001) and the placebo group (P ≤ 0.02). Exercise reduced peak isometric torque (i.e. 9–19% relative to baseline; P ≤ 0.001), which persisted for the first 48 h of recovery with no difference between treatment groups. In contrast, changes in the urine concentration of F₂-isoprostanes responded differently to each treatment (P = 0.04), with a tendency for higher concentrations after 48 h of recovery in the supplemented group (6.2 ± 6.1 vs. 3.7 ± 3.4 ng ml⁻¹). Vitamin C & E supplementation also affected serum cortisol concentrations, with an attenuated increase from baseline to the peak values reached after 1 h of recovery compared with the placebo group (P = 0.02) and serum interleukin-6 concentrations were higher after 1 h of recovery in the antioxidant group (11.3 ± 3.4 pg ml⁻¹) than the placebo group (6.2 ± 3.8 pg ml⁻¹; P = 0.05). Combined vitamin C & E supplementation neither reduced markers of oxidative stress or inflammation nor did it facilitate recovery of muscle function after exercise-induced muscle damage.     

Carbohydrate gel ingestion significantly improves the intermittent endurance capacity, but not sprint performance, of adolescent team games players during a simulated team games protocol

The aim of this study was to investigate the influence of ingesting a carbohydrate (CHO) gel on the intermittent endurance capacity and sprint performance of adolescent team games players. Eleven participants [mean age 13.5 ± 0.7 years, height 1.72 ± 0.08 m, body mass (BM) 62.1 ± 9.4 kg] performed two trials separated by 3–7 days. In each trial, they completed four 15 min periods of part A of the Loughborough Intermittent Shuttle Test (LIST), followed by an intermittent run to exhaustion (part B). In the 5 min pre-exercise, participants consumed 0.818 mL kg⁻¹ BM of a CHO or a non-CHO placebo gel, and a further 0.327 mL kg⁻¹ BM every 15 min during part A of the LIST (38.0 ± 5.5 g CHO h⁻¹ in the CHO trial). Intermittent endurance capacity was increased by 21.1% during part B when the CHO gel was ingested (4.6 ± 2.0 vs. 3.8 ± 2.4 min, P < 0.05, r = 0.67), with distance covered in part B significantly greater in the CHO trial (787 ± 319 vs. 669 ± 424 m, P < 0.05, r = 0.57). Gel ingestion did not significantly influence mean 15 m sprint time (P = 0.34), peak sprint time (P = 0.81), or heart rate (P = 0.66). Ingestion of a CHO gel significantly increases the intermittent endurance capacity of adolescent team games players during a simulated team games protocol.     

Serum oxidant and antioxidant status during early and late recovery periods following an all-out 21-km run in trained adolescent runners

It is well documented that intense exercise precipitates oxidative stress in adults. However, there is lack of related studies concerning oxidant and antioxidant status during early and late recovery periods in adolescent athletes, following endurance exercise in particular. This study investigated aspects of the serum oxidant and antioxidant status of 12 male adolescent (16.2 ± 0.6 years) trained runners during early and late recovery periods after an all-out 21-km run. Venous blood samples were taken immediately before, 2 and 4 h following (early recovery period), and 24 h following (late recovery period) the 21-km run. Samples were analyzed for serum concentrations of thiobarbituric acid-reactive substances (TBARS), uric acid (UA), reduced glutathione (GSH), and enzymatic activity of xanthine oxidase (XO), superoxide dismutase (SOD), and catalase (CAT). During the early recovery period, there were increases in the 4-h GSH (194.8 ± 10.4 vs. 211.8 ± 11.4 mg l⁻¹, P < 0.05), 2- and 4-h UA (307.8 ± 68.6 vs. 327.4 ± 63.8; 330.2 ± 65.1 μmol l⁻¹, P < 0.05), and 2-h CAT (2.05 ± 0.44 vs. 3.07 ± 0.51 U ml⁻¹, P < 0.05), and decreases in the 2-h XO (11.1 ± 1.5 vs. 10.3 ± 1.2 U l⁻¹, P < 0.05) compared to the corresponding pre-exercise level, respectively. No change was observed in SOD (P > 0.05). At the late recovery period, there was an increase in CAT (2.80 ± 0.49 U ml⁻¹, P < 0.05) and TBARS (2.99 ± 0.83 vs. 4.40 ± 1.38 nmol ml⁻¹, P < 0.05). These data indicate that although the antioxidant capacity of adolescent runners is augmented during the early recovery period following the 21-km run, they were not completely protected from oxidative stress during the later recovery period.     

Plasma vasopressin,renin activity,and aldosterone responses to maximal exercise in active college females

Summary The effect of maximal treadmill exercise on plasma concentrations of vasopressin (AVP); renin activity (PRA); and aldosterone (ALDO) was studied in nine female college basketball players before and after a 5-month basketball season. Pre-season plasma AVP increased (p<0.05) from a pre-exercise concentration of 3.8±0.5 to 15.8±4.8 pg · ml⁻¹ following exercise. Post-season, the pre-exercise plasma AVP level averaged 1.5±0.5 pg · ml⁻¹ and increased to 16.7±5.9 pg · ml⁻¹ after the exercise test. PRA increased (p<0.05) from a pre-exercise value of 1.6±0.6 to 6.8±1.7 ngAI · ml⁻¹ · hr⁻¹ 5 min after the end of exercise during the pre-season test. In the post-season, the pre-exercise PRA was comparable (2.4±0.6 ngAI · ml⁻¹ · hr⁻¹), as was the elevation found after maximal exercise (8.3±1.9 ngAI · ml⁻¹ · hr⁻¹). Pre-season plasma ALDO increased (p<0.05) from 102.9±30.8 pg · ml⁻¹ in the pre-exercise period to 453.8±54.8 pg · ml⁻¹ after the exercise test. In the post-season the values were 108.9±19.4 and 365.9±64.4 pg · ml⁻¹, respectively. Thus, maximal exercise in females produced significant increases in plasma AVP, renin activity, and ALDO that are comparable to those reported previously for male subjects. Moreover, this response is remarkably reproducible as demonstrated by the results of the two tests performed 5 months apart.     

Complete correction of anemia by erythropoiesis-stimulating agents is associated with insulin resistance in hemodialysis patients

Insulin resistance and anemia secondary to erythropoietin deficiency characterize patients with end-stage kidney disease. In a cross-sectional analysis, we examined the relationship between erythropoietin-mediated correction of anemia and insulin sensitivity in nondiabetic hemodialysis patients. Insulin sensitivity (euglycemic-hyperinsulinemic clamp) and endogenous glucose production (primed-continuous infusion of [6,6-²H₂]glucose) were determined in two groups of patients with normal hemoglobin (n:8; mean hemoglobin: 14.0 ± 0.3 g/dl) or with mild anemia (n:10; mean hemoglobin: 12.1 ± 0.9 g/dl). The patients with normal hemoglobin were receiving higher (P < 0.05) erythropoietin doses than those with mild anemia (171 ± 73 and 91 ± 39 U kg⁻¹ wk⁻¹, respectively). The two groups were matched for all other potential determinants of insulin resistance. Endogenous glucose production was similar in the two groups of patients in the postabsorptive state and was completely suppressed by insulin infusion. During the hyperinsulinemic clamp, the rate of glucose infusion to maintain euglycemia was significantly lower (P < 0.01) in the patients with normal hemoglobin levels [166 ± 31 mg (m²)⁻¹ min⁻¹] than in those with mild anemia [251 ± 49 mg (m²)⁻¹ min⁻¹] and in a group of matched controls [275 ± 68 mg (m²)⁻¹ min⁻¹]. In pooled patients, individual values of hemoglobin concentrations inversely correlated with the rates of insulin-mediated glucose infusion, both as absolute values (r = −0.58; P < 0.05) and as values normalized by steady-state plasma insulin concentration (r = −0.74; P < 0.001). In conclusion, this exploratory study indicates that complete correction of anemia by erythropoietin treatment in patients with end-stage kidney disease on hemodialysis is associated with impaired insulin sensitivity.     

Post-exercise protein synthesis rates are only marginally higher in type I compared with type II muscle fibres following resistance-type exercise

We examined the effect of an acute bout of resistance exercise on fractional muscle protein synthesis rates in human type I and type II muscle fibres. After a standardised breakfast (31 ± 1 kJ kg⁻¹ body weight, consisting of 52 Energy% (En%) carbohydrate, 34 En% protein and 14 En% fat), 9 untrained men completed a lower-limb resistance exercise bout (8 sets of 10 repetitions leg press and leg extension at 70% 1RM). A primed, continuous infusion of l-[ring-¹³C₆]phenylalanine was combined with muscle biopsies collected from both legs immediately after exercise and after 6 h of post-exercise recovery. Single muscle fibres were dissected from freeze-dried biopsies and stained for ATPase activity with pre-incubation at a pH of 4.3. Type I and II fibres were separated under a light microscope and analysed for protein-bound l-[ring-¹³C₆]phenylalanine labelling. Baseline (post-exercise) l-[ring-¹³C₆]phenylalanine muscle tissue labelling, expressed as (∂¹³C/¹²C), averaged −32.09 ± 0.28, −32.53 ± 0.10 and −32.02 ± 0.16 in the type I and II muscle fibres and mixed muscle, respectively (P = 0.14). During post-exercise recovery, muscle protein synthesis rates were marginally (8 ± 2%) higher in the type I than type II muscle fibres, at 0.100 ± 0.005 versus 0.094 ± 0.005%/h, respectively (P < 0.05), whereby rates of mixed muscle protein were 0.091 ± 0.005%/h. Muscle protein synthesis rates following resistance-type exercise are only marginally higher in type I compared with type II muscle fibres.     

The impact of exercise intensity on the release of cardiac biomarkers in marathon runners

We sought to determine the influence of exercise intensity on the release of cardiac troponin I (cTnI) and N-terminal pro-brain natriuretic peptide (NT-proBNP) in amateur marathon runners. Fourteen runners completed three exercise trials of the same duration but at exercise intensities corresponding to: (a) a competitive marathon [mean ± SD: heart rate 159 ± 7 beat min⁻¹, finish time 202 ± 14 min]; (b) 95% of individual anaerobic threshold [heart rate 144 ± 6 beat min⁻¹] and; (c) 85% of individual anaerobic threshold [heart rate 129 ± 5 beat min⁻¹]. cTnI and NT-proBNP were assayed from blood samples collected before, 30 min and 3 h post-exercise for each trial. cTnI and NT-proBNP were not different at baseline before each trial. After exercise at 85% of individual anaerobic threshold cTnI was not significantly elevated. Conversely, cTnI was elevated after exercise at 95% of individual anaerobic threshold (0.016 μg L⁻¹) and to an even greater extent after exercise at competition intensity (0.054 μg L⁻¹). Peak post-exercise values of NT-proBNP were elevated to a similar extent after all exercise trials (P < 0.05). The upper reference limit for cTnI (0.04 μg L⁻¹) was exceeded in six subjects at competition intensity. No data for NT-proBNP surpassed its upper reference limit. Peak post-exercise values for cTnI and NT-proBNP were correlated with their respective baseline values. These data suggest exercise intensity influences the release of cTnI, but not NT-proBNP, and that competitive marathon running intensity is required for cTnI to be elevated over its upper reference limit.     

Combined carbohydrate-protein supplementation improves competitive endurance exercise performance in the heat

Laboratory-based studies have demonstrated that adding protein (PRO) to a carbohydrate (CHO) supplement can improve thermoregulatory capacity, exercise performance and recovery. However, no study has investigated these effects in a competitive sporting context. This study assessed the effects of combined CHO–PRO supplementation on physiological responses and exercise performance during 8 days of strenuous competition in a hot environment. Twenty-eight cyclists participating in the TransAlp mountain bike race were randomly assigned to fitness-matched placebo (PLA 76 g L⁻¹ CHO) or CHO–PRO (18 g L⁻¹ PRO, 72 g L⁻¹ CHO) groups. Participants were given enough supplements to allow ad libitum consumption. Physiological and anthropometric variables were recorded pre- and post-exercise. Body mass decreased significantly from race stage 1 to 8 in the PLA group (−0.75 ± 0.22 kg, P = 0.01) but did not change in the CHO–PRO group (0.42 ± 0.42 kg, P = 0.35). Creatine kinase concentration and muscle soreness were substantially elevated during the race, but were not different between groups (P = 0.82, P = 0.44, respectively). Urine osmolality was significantly higher in the CHO–PRO versus the PLA group (P = 0.04) and the rise in tympanic temperature from pre- to post-exercise was significantly less in CHO–PRO versus PLA (P = 0.01). The CHO–PRO group also completed the 8 stages significantly quicker than the PLA group (2,277 ± 127 vs. 2,592 ± 68 min, respectively, P = 0.02). CHO–PRO supplementation therefore appears to prevent body mass loss, enhance thermoregulatory capacity and improve competitive exercise performance despite no effect on muscle damage.     

High-intensity exercise decreases muscle buffer capacity via a decrease in protein buffering in human skeletal muscle

We have previously reported an acute decrease in muscle buffer capacity (βm_{in vitro}) following high-intensity exercise. The aim of this study was to identify which muscle buffers are affected by acute exercise and the effects of exercise type and a training intervention on these changes. Whole muscle and non-protein βm_{in vitro} were measured in male endurance athletes (VO_2max = 59.8 ± 5.8 mL kg⁻¹ min⁻¹), and before and after training in male, team-sport athletes (VO_2max = 55.6 ± 5.5 mL kg⁻¹ min⁻¹). Biopsies were obtained at rest and immediately after either time-to-fatigue at 120% VO_2max (endurance athletes) or repeated sprints (team-sport athletes). High-intensity exercise was associated with a significant decrease in βm_{in vitro} in endurance-trained males (146 ± 9 to 138 ± 7 mmol H⁺·kg d.w.⁻¹·pH⁻¹), and in male team-sport athletes both before (139 ± 9 to 131 ± 7 mmol H⁺·kg d.w.⁻¹·pH⁻¹) and after training (152 ± 11 to 142 ± 9 mmol H⁺·kg d.w.⁻¹·pH⁻¹). There were no acute changes in non-protein buffering capacity. There was a significant increase in βm_{in vitro} following training, but this did not alter the post-exercise decrease in βm_{in vitro}. In conclusion, high-intensity exercise decreased βm_{in vitro} independent of exercise type or an interval-training intervention; this was largely explained by a decrease in protein buffering. These findings have important implications when examining training-induced changes in βm_{in vitro}. Resting and post-exercise muscle samples cannot be used interchangeably to determine βm_{in vitro}, and researchers must ensure that post-training measurements of βm_{in vitro} are not influenced by an acute decrease caused by the final training bout.     

Diurnal variation in the salivary melatonin responses to exercise: relation to exercise-mediated tachycardia

Salivary melatonin concentration is an established marker of human circadian rhythmicity. It is thought that melatonin is relatively robust to the masking effects of exercise. Nevertheless, the extent and even the direction of exercise-related change is unclear, possibly due to between-study differences in the time of day exercise is completed. Therefore, we aimed to compare melatonin responses between morning and afternoon exercise, and explore the relationships between exercise-related changes in melatonin and heart rate. At 08:00 and 17:00 hours, seven male subjects (mean ± SD age, 27 ± 5 years) completed 30 min of cycling at 70% peak oxygen uptake followed by 30 min of rest. Light intensity was maintained at ~150 lx. Salivary melatonin (ELISA) and heart rate were measured at baseline, 15 min during exercise, immediately post-exercise and following 30 min recovery. Melatonin was ≈15 pg ml⁻¹ higher in the morning trials compared with the afternoon (P = 0.030). The exercise-related increase in melatonin was more pronounced (P = 0.024) in the morning (11.1 ± 8.7 pg ml⁻¹) than in the afternoon (5.1 ± 5.7 pg ml⁻¹). The slope of the heart rate–melatonin relationship was significantly (P = 0.020) steeper in the morning (0.12 pg ml⁻¹ beats⁻¹ min⁻¹) than in the afternoon (0.03 pg ml⁻¹ beats⁻¹ min⁻¹). In conclusion, we report for the first time that the masking effect of moderate-intensity exercise on melatonin is approximately twice as high in the morning than the afternoon. The much steeper relationship between heart rate and melatonin changes in the morning raises the possibility that time of day alters the relationships between exercise-mediated sympathetic nervous activity and melatonin secretion.     

Influence of moderate hypoxia on tolerance to high-intensity exercise

It remains uncertain as how the reduction in systemic oxygen transport limits high-intensity exercise tolerance. 11 participants (5 males; age 35 ± 10 years; peak [(V)\dot]\textO₂ max {\dot{V}\text{O}}_{2} \max 3.5 ± 0.4 L min⁻¹) performed cycle ergometry to the limit of tolerance: (1) a ramp test to determine ventilatory threshold (VT) and peak [(V)\dot]\textO₂ {\dot{V}\text{O}}_{2} ; (2) three to four constant-load tests in order to model the linear P–t ⁻¹ relationship for estimation of intercept (critical power; CP) and slope (AWC). All tests were performed in a random order under moderate hypoxia (FiO₂ = 0.15) and normoxia. The linearity of the P–t ⁻¹ relationship was retained under hypoxia, with a systematic reduction in CP (220 ± 25 W vs. 190 ± 28 W; P < 0.01) but no significant difference in AWC (11.7 ± 5.5 kJ vs. 12.1 ± 4.4 kJ; P > 0.05). However, large individual variations in the change of the latter were observed (−36 to +66%). A significant relationship was found between the % change in CP (r = 0.80, P < 0.01) and both peak [(V)\dot]\textO₂ {\dot{V}\text{O}}_{2} (CP: r = −0.65, P < 0.05) and VT values recorded under normoxia (CP: r = −0.65, P < 0.05). The present study demonstrates the aerobic nature of the intercept of the P–t ⁻¹ relationship, i.e. CP. However, the extreme within-individual changes in AWC do not support the original assumption that AWC reflects a finite energy store. Lower hypoxia-induced decrements in CP were observed in aerobically fitter participants. This study also demonstrates the greater ability these participants have to exercise at supra-CP but close to CP workloads under moderate hypoxia.     

The relationship between monocarboxylate transporters 1 and 4 expression in skeletal muscle and endurance performance in athletes

The purpose of this study was to examine the relationship between skeletal muscle monocarboxylate transporters 1 and 4 (MCT1 and MCT4) expression, skeletal muscle oxidative capacity and endurance performance in trained cyclists. Ten well-trained cyclists (mean ± SD; age 24.4 ± 2.8 years, body mass 73.2 ± 8.3 kg, VO_2max 58 ± 7 ml kg⁻¹ min⁻¹) completed three endurance performance tasks [incremental exercise test to exhaustion, 2 and 10 min time trial (TT)]. In addition, a muscle biopsy sample from the vastus lateralis muscle was analysed for MCT1 and MCT4 expression levels together with the activity of citrate synthase (CS) and 3-hydroxyacyl-CoA dehydrogenase (HAD). There was a tendency for VO_2max and peak power output obtained in the incremental exercise test to be correlated with MCT1 (r = −0.71 to −0.74; P < 0.06), but not MCT4. The average power output (P _average) in the 2 min TT was significantly correlated with MCT4 (r = −0.74; P < 0.05) and HAD (r = −0.92; P < 0.01). The P _average in the 10 min TT was only correlated with CS activity (r = 0.68; P < 0.05). These results indicate the relationship between MCT1 and MCT4 as well as cycle TT performance may be influenced by the length and intensity of the task.     

Effect of exercise on glutamine metabolism in macrophages of trained rats

This study investigated the effect of exercise on glutamine metabolism in macrophages of trained rats. Rats were divided into three groups: sedentary (SED); moderately trained (MOD) rats that were swim trained 1 h/day, 5 days/week for 6 weeks; and exhaustively trained (EXT) rats that were similarly trained as MOD for 5 weeks and, in the 6th week, trained in three 1-h sessions/day with 150 min of rest between sessions. The animals swam with a load equivalent to 5.5% of their body weight and were killed 1 h after the last exercise session. Cells were collected, and glutamine metabolism in macrophage and function were assayed. Exercise increased phagocytosis in MOD when compared to SED (34.48 ± 1.79 vs 15.21 ± 2.91%, P < 0.05); however, H₂O₂ production was higher in MOD (75.40 ± 3.48 nmol h × 10⁵ cell⁻¹) and EXT (79.20 ± 1.18 nmol h × 10⁵ cell⁻¹) in relation to SED (32.60 ± 2.51 nmol h × 10⁵ cell⁻¹, P < 0.05). Glutamine consumption increased in MOD and EXT (26.53 ± 3.62 and 19.82 ± 2.62 nmol h × 10⁵ cell⁻¹, respectively) relative to SED (6.72 ± 0.57 nmol h × 10⁵ cell⁻¹, P < 0.05). Aspartate increased in EXT (9.72 ± 1.14 nmol h × 10⁵ cell⁻¹) as compared to SED (1.10 ± 0.19 nmol h × 10⁵ cell⁻¹, P < 0.05). Glutamine decarboxylation was increased in MOD (12.10 ± 0.27 nmol h × 10⁵ cell⁻¹) and EXT (16.40 ± 2.17 nmol h × 10⁵ cell⁻¹) relative to SED (1.10 ± 0.06 nmol h × 10⁵ cell⁻¹, P < 0.05). This study suggests an increase in macrophage function post-exercise, which was supported by enhanced glutamine consumption and metabolism, and highlights the importance for glutamine after exercise.     

Influence of menstrual cycle phase on pulmonary function in asthmatic athletes

The main aim of this study was to investigate whether there is a relationship between menstrual cycle phase and exercise-induced bronchoconstriction (EIB) in female athletes with mild atopic asthma. Seven eumenorrheic subjects with regular 28-day menstrual cycles were exercised to volitional exhaustion on day 5 [mid-follicular (FOL)] and day 21 [mid-luteal (LUT)] of their menstrual cycle. Pulmonary function tests were conducted pre- and post-exercise. The maximal percentage decline in post-exercise forced expiratory volume in 1 s (FEV₁) and forced expiratory flow from 25 to 75% of forced vital capacity (FEF_25–75%) was significantly greater (P<0.05) on day 21 (mid-LUT phase) (−17.35±2.32 and −26.28±6.04%, respectively), when salivary progesterone concentration was highest, compared to day 5 (mid-FOL phase) (−12.81±3.35 and −17.23±8.20%, respectively), when salivary progesterone concentration was lowest. The deterioration in the severity of EIB during the mid-LUT phase was accompanied by worsening asthma symptoms and increased bronchodilator use. There was a negative correlation between the percent change in pre- to post-exercise FEV₁ and salivary progesterone concentration. However, no such correlation was found between salivary estradiol and the percentage change in pre- to post-exercise FEV₁. This study has shown for the first time that menstrual cycle phase is an important determinant of the severity of EIB in female athletes with mild atopic asthma. Female asthmatic athletes may need to adjust their training and competition schedules to their menstrual cycle and to consider the potential negative effects of the LUT phase of the menstrual cycle on exercise performance.     

Carbohydrate ingestion and pre-cooling improves exercise capacity following soccer-specific intermittent exercise performed in the heat

Ingestion of carbohydrate and reducing core body temperature pre-exercise, either separately or combined, may have ergogenic effects during prolonged intermittent exercise in hot conditions. The aim of this investigation was to examine the effect of carbohydrate ingestion and pre-cooling on the physiological responses to soccer-specific intermittent exercise and the impact on subsequent high-intensity exercise performance in the heat. Twelve male soccer players performed a soccer-specific intermittent protocol for 90 min in the heat (30.5°C and 42.2% r.h.) on four occasions. On two occasions, the participants underwent a pre-cooling manoeuvre. During these sessions either a carbohydrate–electrolyte solution (CHOc) or a placebo was consumed at (PLAc). During the remaining sessions either the carbohydrate–electrolyte solution (CHO) or placebo (PLA) was consumed. At 15-min intervals throughout the protocol participants performed a mental concentration test. Following the soccer-specific protocol participants performed a self-chosen pace test and a test of high-intensity exercise capacity. The period of pre-cooling significantly reduced core temperature, muscle temperature and thermal sensation (P < 0.05). Self-chosen pace was greater with CHOc (12.5 ± 0.5 km h⁻¹) compared with CHO (11.3 ± 0.4 km h⁻¹), PLA (11.3 ± 0.4 km h⁻¹) and PLAc (11.6 ± 0.5 km h⁻¹) (P < 0.05). High-intensity exercise capacity was improved with CHOc and CHO when compared with PLA (CHOc; 79.8 ± 7 s, CHO; 72.1 ± 5 s, PLAc; 70.1 ± 8 s, PLA; 57.1 ± 5 s; P < 0.05). Mental concentration during the protocol was also enhanced during CHOc compared with PLA (P < 0.05). These results suggest pre-cooling in conjunction with the ingestion of carbohydrate during exercise enhances exercise capacity and helps maintain mental performance during intermittent exercise in hot conditions.